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PubMed1976

B-lymphocyte alloantigens associated with multiple sclerosis.

6 B-lymphocyte alloantigens have been provisionally identified with lymphocytotoxic antisera reacting, after absorption, specifically with B but not T cells. 3 of these antigens appear to form part of an allelic series. The frequency of HLA and B-lymphocyte antigens was then studied in 59 patients with multiple sclerosis (M.S.). 1 of the B-cell antigens, BT 101, was found in 49 out of 59 patients (83%), compared with 10 out of 30 normal individuals (33%), giving a relative risk of 9-8 times to the association. 2 other B-cell alloantigens and HLA-B7 showed lesser but significant positive associations with M.S. Apart from providing possible clues to the pathogenesis of M.S., the association between BT 101 and M.S. may allow screening for susceptible individuals who are thought to be at special risk.

Adolescent↗
PubMed1977

Renal transplantation and a positive serological cross-match.

A renal transplant involving a recipient with a positive serological cross-match against donor lymphocytes generally results in hyperacute rejection of the graft. 13 cadaveric renal transplants were performed in recipients with a known positive serologic cross-match against donor B lymphocytes. 12 of these serological cross-matches were positive against donor blood, node, or spleen lymphocytes, but the reactivity was directed against donor B lymphocytes only. 3 transplants failed, 2 because of rejection and 1 because of renal-artery thrombosis. 10 transplants are functioning, 6 to 42 weeks after the operation. Of these 10 successful grafts, 3 had no acute rejection episodes, while 7 had an early acute rejection episode which responded to treatment. Histologically, the grafts showed a cellular rejection, similar to that in enhanced renal allografts in the rat. It is possible to transplant a kidney in a high-risk patient with a positive B lymphocyte cross-match with a low risk of failure. In addition active enhancement of the graft might sometimes occur.

Acute Disease↗
PubMed1998

Impact of the MHC-encoded HLA-DMA, DMB, and LMP2 gene polymorphisms on kidney graft outcome.

We previously studied the relationship between TAP1 and TAP2 gene polymorphism and compatibility in kidney graft outcome and reported that the currently described TAP1 and TAP2 gene polymorphisms did not influence the incidence of acute rejection episodes. In this study, we report on the effect of polymorphism and matching of HLA-DMA, -DMB, and LMP2 genes on kidney graft outcome. This study was performed on 102 selected kidney recipients who experienced two or more acute rejection episodes (rejection group) during follow up and who were compared to a group of 150 patients who never had rejection (non rejection group). Although a significant effect of HLA-DR matching was observed between these two groups, our data suggest that matching for all the new genes located in the HLA class II region (TAP1, TAP2, LMP2, HLA-DMA and -DMB) does not influence the kidney graft outcome. However, a significant increase (pc < 0.05) of DMA*0102 allele was observed in the recipients of the rejection group as compared to those of the non rejection group. This effect was not due to a linkage disequilibrium between DMA and HLA-DR loci and suggests that this specific HLA-DMA allele could play a role in the indirect pathway of class II presentation of donor antigens.

Adult↗
PubMed1996

Minor H, rather than MHC, alloantigens offer the greater barrier to successful orthotopic corneal transplantation in mice.

Irrespective of HLA matching, a far higher proportion of human corneal allografts placed orthotopically in avascular corneal graft beds are accepted indefinitely, compared to other types of solid tissue allografts. However, many more corneal grafts are rejected if they are transplanted onto neovascularized recipient eyes. Using a murine model of orthotopic corneal transplantation in which grafts were placed in normal eyes, we have reported previously that grafts bearing minor H antigens alone are more likely to be rejected (approximately 50%) than are grafts displaying only MHC alloantigens (< 20%). Moreover, recipients of MHC plus minor H incompatible corneal grafts developed delayed hypersensitivity (DH) directed solely at minor H antigens. These studies have now been extended to include corneal grafts placed in neovascularized recipient eyes. Neovascularization was induced by placing sutures in the central cornea of one eye of BALB/c mice. Two weeks later corneas from C57BL/10 donors were grafted into these eyes. Rejection reactions were first apparent within 7 days and all grafts were destroyed by 14 days. Donor-specific DH responses were examined by injecting irradiated donor antigen-bearing spleen cells into the ear pinna. To distinguish DH directed at MHC versus minor antigens, some graft recipients were ear-challenged with BALB.B cells (donor MHC only), while other received B10.D2 cells (donor minor H only). Intense ear-swelling responses were evoked by B10.D2 cells, but not by BALB.B cells. These findings indicate that, for orthotopic corneal allografts, minor H antigens offer a more formidable barrier to graft acceptance than do MHC-encoded antigens. We speculate that this unexpected outcome may reflect a reduced level of MHC expression on corneal tissue. Moreover since the cornea lacks bone marrow derived dendritic cells, allorecognition by recipient T cells must occur via the indirect pathway, and in this situation minor H antigens may compete favorably with MHC antigens for processing and presentation by recipient antigen-presenting cells.

Animals↗
PubMed2000

Major histocompatibility complex (MHC)-linked microsatellite markers in a founder population.

The Finnish population is genetically relatively homogeneous and has a narrow gene pool as a result of founder effect followed by rapid population growth. We here demonstrate that microsatellite markers are highly informative tools for major histocompatibility complex (MHC) analysis in this population. First, no variation in 12 MHC-linked microsatellites could be observed in certain CYP21-deficient chromosomes, which as a result of founder effect most likely derived from common ancestors. Second, amongst 131 Finnish chromosomes, some, but not all, apparently HLA-identical chromosomes also carried identical microsatellites, suggesting that these loci could be applied for identification of haplotypes which have a relatively recent shared origins. Finally, when the microsatellites were studied between ethnically more distant individuals (Finnish vs. non-Finnish), who were matched for the HLA alleles, much more differences were observed. This showed that the similarity in microsatellites was population specific. The microsatellite typing can therefore be informative in fine mapping MHC-linked susceptibility genes and can help in matching bone marrow transplants in isolated populations. Linkage disequilibrium was found to be much higher in the MHC than in another region (5q31) of similar size, indicating that there may be particular mechanisms keeping the MHC haplotypes conserved.

Bone Marrow Transplantation↗
PubMed1999

Tetrameric HLA class I-minor histocompatibility antigen peptide complexes demonstrate minor histocompatibility antigen-specific cytotoxic T lymphocytes in patients with graft-versus-host disease.

Graft-versus-host disease (GvHD) is a chief complication of allogeneic bone marrow transplantation. In HLA-identical bone marrow transplantation, GvHD may be induced by disparities in minor histocompatibility antigens (mHags) between the donor and the recipient, with the antigen being present in the recipient and not in the donor. Cytotoxic T lymphocytes (CTLs) specific for mHags of the recipients can be isolated from the blood of recipients with severe GvHD (ref. 3). A retrospective study demonstrated an association between mismatch for mHags HA-1, -2, -4 and -5 and the occurrence of GvHD in adult recipients of bone marrow from HLA genotypically identical donors. Tetrameric HLA-peptide complexes have been used to visualize and quantitate antigen-specific CTLs in HIV-infected individuals and during Epstein-Barr virus and lymphocytic choriomeningitis virus infections. Here we show the direct ex vivo visualization of mHag-specific CTLs during GvHD using tetrameric HLA-class and I-mHag HA-1 and HY peptide complexes. In the peripheral blood of 17 HA-1 or HY mismatched marrow recipients, HA-1- and HY-specific CTLs were detected as early as 14 days after bone marrow transplantation. The tetrameric complexes demonstrated a significant increase in HA-1- and HY-specific CTLs during acute and chronic GvHD, which decreased after successful GvHD treatment. HLA class I-mHag peptide tetramers may serve as clinical tools for the diagnosis and monitoring of GvHD patients.

Adult↗
PubMed2003

Recipient mHag-HA1 disparity and aGVHD in thalassemic-transplanted patients.

In order to determine the influence of HA-1 minor histocompatibility antigen mismatch on BMT outcome, we analyzed a pool of 94 thalassemic transplanted patients all selected for the presence of HLA-A(*)0201 allele. The HA-1 typing was performed using SSP analysis. All the patients received bone marrow from HLA-identical MLC nonresponsive siblings. As graft-versus-host-disease (GVHD) prophylaxis, all patients received cyclosporin and short methotrexate. Grades II-IV GVHD occurred in five (33.3%) of the 15 patients with recipient HA-1 disparity compared with 14 (17.7%) of the 79 patients without HA-1 disparity. Despite the higher incidence of acute graft-versus-host-disease (aGVHD) in the group of patients with HA-1 incompatibility, these data were not statistically significant. However, it was interesting to observe that no GVHD developed in any of the 15 cases in which the recipient was HA-1 negative and the donor HA-1 positive.

Adolescent↗
PubMed1996

T cell receptor (TCR) V gene segment use in HLA-typed Japanese healthy subjects.

The expression of 13 different alpha and beta V gene segments of the T cell receptor for antigen (TCR) was examined, using V gene-specific MoAbs, on human peripheral blood T lymphocytes from 32 healthy Japanese subjects. In addition, to examine associations between TCR V gene products and HLA alleles, the HLA class I and class II types of all subjects were serologically determined. The reactivities of the anti-TCR V-specific MoAbs were, with some significant exceptions, similar to those previously described in healthy Caucasian subjects. We found a non-random V gene usage as well as a statistically significant bias of the expression of eight V beta gene products towards the CD4+ subpopulation, and a significant skewness in the usage of V alpha 12 towards the CD8+ population. Some subjects showed increased reactivities (above 10%) of certain MoAbs, mainly in the CD8+ subpopulation. We found no distinct correlation between any certain HLA class I or II allele and TCR V gene usage in the CD8+ or CD4+ subpopulations, respectively. In conclusion, the pattern of anti-TCR V-specific MoAb reactivities found in CD4+ and CD8+ subsets of peripheral blood lymphocytes of healthy Japanese subjects was in general found to match that previously described in healthy Caucasian subjects.

Adult↗
PubMed2001

HLA typing and immunological characterization of young-onset diabetes mellitus in a Hong Kong Chinese population.

AIMS: A study of the Hong Kong Chinese showed that the majority of subjects with young-onset diabetes (age of diagnosis < 35 years) present with a phenotype suggestive of Type 2 diabetes mellitus, although up to 50% subsequently need insulin treatment. The aim of this study was to use a combination of clinical, genetic and immunological markers to characterize the disease phenotype further in such individuals and to determine whether the requirement for insulin is the result of autoimmune disease. METHODS: One hundred and thirty-seven Hong Kong Chinese with young-onset diabetes were studied, irrespective of their mode of presentation. The subjects were typed for alleles of the HLA-DR and -DQ genes and investigated for the presence of autoantibodies to glutamic acid decarboxylase (GAD). Plasma C-peptide concentration and requirement for insulin were also determined. RESULTS: One hundred and three subjects presented with a syndrome resembling Type 2 diabetes, while 34 presented with Type 1 diabetes. Of the former group, 35 patients (34.0%) were insulin-deficient, 16 (15.5%) were insulin-treated and seven (6.9%) were positive for GAD autoantibodies. Among the GAD-positive subjects presenting with Type 2 diabetes, the HLA-DRB1*03 allele may be a marker of early progression to insulin therapy. CONCLUSIONS: Seven subjects with Type 2 diabetes at presentation had autoantibodies to GAD. Causes other than GAD autoimmunity, however, must be sought to explain the high prevalence of insulin deficiency observed in the Chinese patients. This study highlights the heterogeneity of the pathogenic processes leading to the diabetic phenotype.

Adolescent↗
PubMed2002

TAP, HLA-DQB1, and HLA-DRB1 polymorphism in Colombian patients with primary Sjögren's syndrome.

OBJECTIVE: Although primary Sjögren's syndrome (pSS) has a worldwide distribution, little data is available on pSS immunogenetics in non-white populations. Thus, we investigated the influence of transporters associated with antigen processing (TAP), human leukocyte antigen (HLA)-DQB1, and HLA-DRB1 gene polymorphism in mestizo Colombian patients with pSS. METHODS: In this cross-sectional and controlled study, all patients met the European criteria for classification of pSS. TAP and HLA typing was performed by polymerase chain reaction techniques. Genetic data analysis was performed to detect deviations from the expected Hardy-Weinberg (H-W) proportions and to determine the presence of population stratification or subdivision and the existence of linkage disequilibrium between pairs of loci. RESULTS: Seventy-three Colombian patients with pSS (95% women) and 76 healthy controls were studied. Although significant associations were not observed between TAP or HLA polymorphism and disease, strong linkage disequilibrium among the loci TAP2 and DQB1 was found in patients. Deviations from the H-W expected value were found in the DQB1 locus of patients (P =.02). HLA-DRB1*0301-DQB1*0201 haplotype was associated with more severe histopathologic disease (odds ratio [OR], 15.5; 95% confidence interval [CI], 1.9-129; P =.001) and the presence of anti-Ro (OR, 3.8; 95% CI, 1-15; P =.04) and anti-La antibodies (OR, 4.3; 95% CI, 1.3-14; P =.01). CONCLUSION: The data show genetic evidence suggesting that, in Colombians, a region immersed or in the vicinity in the HLA class II system is strongly associated with a predisposition to acquire pSS, which is probably located between the TAP2 and HLA-DQB1 locus. Our results confirm that the HLA-DRB1*0301-DQB1*0201 haplotype participates in the pathogenesis of pSS.

ATP Binding Cassette Transporter, Subfamily B, Mem↗
PubMed1974

Serological distinction of mutants B6.CH(zl) and B6.M505 from strain C57BL-6.

A quantitative serological difference was found between strains Hz1 and M505 carrying mutant H-2 haplotypes ba and bd, respectively, and the original strain B6(H-2(b)). The finding suggests that the mutations occurred in the H-2K(b) gene, and together with data on MLR and CML challenges the current concept of H-2 regions' involvement in immune reactions.

Animals↗
PubMed1996

The role of cell-mediated cytotoxicity in acute GVHD after MHC-matched allogeneic bone marrow transplantation in mice.

The role of cell-mediated cytotoxicity in the complex pathophysiology of graft-versus-host disease (GVHD) has remained poorly defined for several decades. We transplanted T cells from Fas-ligand (FasL)-defective and perforin-deficient mutant donor mice into lethally irradiated MHC-matched allogeneic recipient mice to characterize the role of cell-mediated cytotoxicity in GVHD. Although recipients of allogeneic FasL-defective donor T cells underwent severe GVHD-associated cachexia, they exhibited only minimal signs of hepatic and cutaneous GVHD pathology. Recipients of perforin-deficient allogeneic donor T cells developed signs of acute GVHD, but the time of onset was significantly delayed. These findings demonstrate that Fas-mediated anti-recipient cytotoxicity may be critical for the development of hepatic and cutaneous GVHD, but is not required for GVHD-associated cachexia. In addition, perforin-mediated anti-recipient cytotoxicity appears to play an important role in the kinetics of GVHD pathophysiology, but is not required for GVHD-associated tissue damage.

Animals↗
PubMed1984

Failure to acquire Epstein-Barr virus infection after intimate exposure to the virus.

In 1981, 54 Epstein-Barr virus-seronegative pregnant women in the Sacramento-Davis area of California were observed prospectively for an average duration of 12.1 months for Epstein-Barr virus-seroconversion. Only one seroconverted. Two of the 54 women remained negative for Epstein-Barr virus antibody 4.5-5.0 months after their husbands were proved to be Epstein-Barr virus excreters. Short of experimental pharyngeal introduction of the virus into human volunteers, these data provide the most direct evidence possible that the intimate exposure of Epstein-Barr virus-seronegative adults to the virus does not necessarily result in infection.

Adolescent↗
PubMed1992

Autoimmunity and genetics contribute to the risk of insulin-dependent diabetes mellitus in families: islet cell antibodies and HLA DQ heterodimers.

The risk for insulin-dependent diabetes mellitus (IDDM) associated with genetic susceptibility markers at the human leukocyte antigen (HLA) DQA1 and DQB1 loci was evaluated among individuals with and those without islet cell antibodies. A total of 108 antibody-positive parents and siblings of IDDM patients from the Pittsburgh registry were identified among 1,592 who were screened. HLA-DQ molecular typing was performed on 79 of these individuals and on 78 antibody-negative relatives. There were similar proportions of homozygotes for both of the diabetogenic alleles DQA1 arginine-52 (R/R) and DQB1 non-aspartate-57 (nD/nD) among the antibody-positive and antibody-negative relatives (19.0 and 15.4%, respectively). However, subsequent development of IDDM was restricted to individuals who were both antibody positive and carried the potential to make at least one diabetogenic DQ heterodimer. A dose-response effect was observed among the antibody-positive relatives, in which two of 18 capable of generating one diabetogenic heterodimer and six of 29 generating two heterodimers became insulin requiring. Nine of 15 who were homozygous for both R/R and nD/nD, coding exclusively for diabetogenic variants, became diabetic over the course of the follow-up. With a multivariate model, the relative risk for IDDM among those with islet cell antibodies who were also R/R and nD/nD was estimated to be 229.3 compared with those lacking both, after age and sex were controlled for. The data suggest that while autoimmunity, indicated by the presence of cytoplasmic islet cell antibodies may be relatively common, it progresses only in those with variant HLA-DQ molecules.

Adolescent↗